羟基酪醇对过度训练大鼠心肌线粒体动力学蛋白及自噬水平的影响
Effects of hydroxytyrosol on myocardial mitochondrial dynamic protein and autophagy in the excessive exercise rats
投稿时间:2014-01-19  修订日期:2014-01-19
DOI:
中文关键词:  过度训练  心肌  生物合成  裂解  融合  自噬
英文关键词:excessive training  myocardium  biosynthesis  fission  fusion  autophagy
基金项目:国家青年科学基金资助项目(81100174)。 ,殷红2
作者单位E-mail
孙云彦 南阳理工学院体育教学部;河南大学体育学院 sunyy1888@163.com 
殷红 河南大学体育学院  
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中文摘要:
      目的: 作为一种天然的线粒体营养素,羟基酪醇(HT)对心血管疾病具有优越的治疗效果。但其对过度训练(ET)后心肌线粒体的影响及机制尚不清楚。本研究检测了ET后心肌线粒体功能,观察HT对线粒体功的保护效应,并通过关注动力学及自噬蛋白变化,探讨HT保护机制。方法:80只Sprague dawley大鼠随机分成4组,即:正常对照组(CON),正常加羟基酪醇组(CON HT),过度训练组(ET)及训练加羟基酪醇组(ET HT)。灌胃给药,剂量为25mg/kg/d。每周训练时间为周一至周六,共8周。氧耗法测定线粒体呼吸功能。Westerblot法检测线粒体生物合成(PGC-1α),复合物(I,II,III,IV,V),动力学(融合:Mfn1/2,OPA1;裂解:Drp1)及自噬相关蛋白(Atg5,Beclin-1及Lc3-B)。结果: ET可显著性降低线粒体呼吸控制率(RCR)及磷氧比值(P/O),下调PGC-1α及复合物I,IV,V表达,增加线粒体裂解(Drp1),降低融合 (Mfn2,Opa1)。相对地,HT可有效提高线粒体P/O及复合物I,V表达水平;促进生物合成(Pgc-1α),提高融合(Mfn2,Opa1),降低裂解(Drp1)和自噬 (Atg5,Lc3-B)。结论:ET造成的心肌线粒体功能异常与动力学蛋白及自噬水平变化相关。HT对上述病理性变化的抑制作用可能是其发挥保护作用的重要机制。
英文摘要:
      Objective:Hydroxytyrosol (HT), one natural mitochondrial nutrient, has been reported to exert beneficial effects on cardiovascular-associated diseases. However, the effects and underlying molecular mechanisms of HT on excessive training (ET) -induced mitochondrial dysfunctions were still unclear. In the current study, we have evaluated the changes of mitochondrial respiratory functions, alterations of mitochondrial dynamics and autophagy related proteins, through which explored HT-induced favorable protections for myocardium in the excessive training animas. Methods: 80 Sprague dawley rats were subjected to this experiment and were divided into four groups: sedentary group (CON); sedentary HT group (CON HT); excessive exercise training group (ET) and ET HT group. Administration regimen: 25mg/kg/d. Training from Monday to Friday each week, a total of eight weeks. Oxygen consumption was used for evaluating mitochondrial respiratory functions. Westerblot were used to determine mitochondrial biogenesis (Pgc-1α), complexes protein expressions, mitochondrial dynamics (fusion: Mfn1/2, Opa1; fission: Drp1) and autophagy associated proteins (atg5, beclin-1and lc3-B). Results: ET was showed to significantly decrease mitochondrial respiratory control rate (RCR) and value of P/O, downregulate PGC-1α and complex I, IV and V levels. ET also was revealed to induce mitochondrial dynamics pathological remodelling (increased fission [Drp1] and decreased fusion [Mf2 and Opa1]) and elevate autophagy level (Atg5,Beclin-1). HT treatment was found to efficiently increase P/O, complex I, V levels, which were indicated to involve in increased protein levels of Pgc-1α, Mfn2, Opa1 and decreased Drp1, Atg5 and Lc3-B. Conclusion: These results demonstrated that ET-induced myocardial mitochondrial dysfunctions may be mediated via the downregulation of mitochondrial biogenesis, dynamic proteins and upregulation of autophagy. HT may normalize mitochondrial dynamic remodeling and decrease autophagy, thereby improving mitochondrial functional performances.
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